The objective of the proposed work is to identify immunological mechanisms responsible for glomerulonephritis and tubulointerstitial nephritis in experimental animals and in man. We will try to establish new models of immunologically-mediated glomerulonephritis induced by exposure of animals to common agents of pollution such as HgCl2. We will study: 1) the morphologic and functional changes induced by antibodies reacting with the brush border of proximal convoluted tubules; 2) the development of antibodies to tubular basement membrane in renal allografts; and, 3) some co-factors which may have importance in the pathogenesis of the hemorrhagic pneumonitis occurring in Goodpasture's syndrome. We will try to verify the existance of comparable mechanisms of immunologically-mediated injury in man. More precise information concerning the mechanisms of these diseases is indispensablein order to devise a better treatment which may reduce the incidence of chronic renal failure, requiring hemodialysis or renal transplantation.